Theories of growth and development

GOOD MORNING
Its not about how hard you hit. It’s
about how hard you can get hit
and keep moving forward; how
much you can take and keep
moving forward. That’s how
winning is done!....
Sylvester Stallone,Rocky Balboa.
1

“GROWTH & DEVELOPMENT”

Theories & Principles

2

CONTENTS
Introduction
 Mechanism of bone growth
 Deposition and Resorption
 Growth fields
 Growth sites
 Growth centers
 Remodeling
 Molecular biology of bone
remodeling


3

 Principle of „Area relocation‟
Enlow V principle

1.
2.

Growth movement
Cortical Drift
Displacement

 Trajectories of bones

1. Trajectories in maxilla
2. Trajectories in mandible
4

Changing concepts & hypothesis of
craniofacial growth1. Evolution of theories
2. The Remodelling theory (Brash
1930s)
3. The Genetic concept (Brodie 1940s)
4. The Sutural hypothesis ( Sicher 1941)

5

5. The Cartilaginous theory (Scott 1950s)
6. The Functional Matrix theory (Moss 1962)
7. Neurotrophism
8. The Cybernetics theory
(AlexandrePetrovic 1970)
9. Conclusion
10. References
6

INTRODUCTION
Growth and development are two integral
process which defines the existence of life.

Growth of an organism is the interplay
between its genetic constitution and
environment in which it thrives.

7

Assessment of growth revels about the
general health of the individual and can
be used for growth modification
treatments.
Growth is a complex process and is not
supported by a single theory but is based to
a large extent on evolving concepts
concerning the biological mechanisms of
craniofacial development.
8

MECHANISM OF BONE GROWTH
Bone growth is based on certain basic
principles .
Bones do not grow symmetrically but
grow by complex differentiation
mechanism .
9

All bone growth is a complicated
mixture of the two basic principles
deposition and resorption .

Deposition and resorption which are

carried out by the growth fields
comprised of the soft tissue investing the
bone.
10

As the fields grows and function differently
on different parts of the bone ,the bone
undergoes remodeling.

When the amount of bone deposition is
greater than the resorption , enlargement of
the bone necessitates its displacement.

11

DEPOSITION AND RESORPTION
Bone grows by addition of new bone
tissue on one side of the bony cortex.
Bone formative changes occurs on the
surface facing towards the direction of
progressive growth resulting in new bone
deposition.
Deposition is observed on the tension
side.

12

+ Bone deposition
- Bone resorption

13

DEPOSITION AT HISTOLOGICAL LEVEL
Bone Cells


Osteoblasts: Bone
generating cell



Osteocytes: Mature
bone cells, spider
shaped and maintain
bone tissue



Osteoclasts: Bone
destroying cells

14

OSTEOBLASTS


Osteoblasts are
responsible for the
synthesis of the organic
components of bone
matrix (type I collagen,
proteoglycans, and
glycoproteins).



Osteoblasts depends
on deposition of the
inorganic components
of bone
15

OSTEOCYTES


Osteocytes, which
derive from
osteoblasts, lie in the
lacunae situated
between lamellae of
matrix.



Only one osteocyte is
found in each lacuna.



Lacunae: spaces
occupied by osteocyte
cell body
17

OSTEOCLASTS


Osteoclasts are
very large and
branched motile
cells.



Dilated portions of
the cell body
contain from 5 to 50
(or more) nuclei.
19

Osteoclasts are
derived from the
mononucleated cells

Active osteoblasts
stimulate osteoclast
activity.
20

BONE REMODELING
 Bone

remodeling involves

independent sites of resorption and

formation that change the size and
shape of a bone.

23

REMODELLING



It involves deposition
and resorption

Four types:
Biomechanical
Growth remodelling


Haversian remodelling

Pathologic remodelling

24

1.Biomechanical- continuous deposition &

removal of ions to maintain mineral
homeostasis
2.Growth remodelling- constant replacement
of bone during childhood
3.Haversian remodelling- secondary process
of cortical reconstruction as primary vascular
bone is replaced.
4.Pathologic remodelling- regeneration &
reconstruction of bone during & following
trauma
25



E.g. The ramus

moves posteriorly
by the
combination of
deposition and
resorption.


So the anterior
part of the ramus
gets remodeled
26

FUNCTIONS OF REMODELING
1.

Progressively change the size of whole bone

2.

Sequentially relocate each component of the
whole bone

3.

Progressively change the shape of the bone
to accommodate its various functions

27

4.

Progressive fine tune fitting of all the
separate bones to each other and to

their contiguous ,growing, functioning
soft tissues.

5. Carry out continuous structural
adjustments to adapt to the intrinsic
and extrinsic changes in conditions .
28

MOLECULAR BIOLOGY OF BONE REMODELLING
Bone remodeling is accomplished according to the
following phases:

1.Activation phase –
Different inputs such as a microfracture , an
alteration of mechanical loading sensed by
the osteocytes or factors released in the
bone microenvironment including IGF-1,
TNF-alfa, IL-6 .PTH, activate the lining
cells ,which are quiescent osteoblast.
29

•As a consequence lining cells increase
their own surface expression of
RANKL(Receptor activator of nuclear
ligand) which in turn interacts with its
receptor RANK , expressed by
preosteoclast .
• RANK / RANKL interaction triggers
preosteoclast fusion and differentiation
towards multinucleated osteoclast.
Rucci, N.: Molecular biology of bone remodelling , Clinical
cases in Mineral and Bone metabolism : 2008;5(1): 49-56
30

2. Resorption phase• Once differentiated osteoclast polarize , adhere
to the bone surface and begin to dissolve bone.
•

This function requires two steps :Acidification of
bone matrix to dissolve inorganic content and
release of lysosomal enzymes such as cathepsin
K and MMP9 both in charge for degradation of
organic content. Once accomplished their
function osteoclast undergo apoptosis.

Rucci, N.: Molecular biology of bone remodelling , Clinical cases
in Mineral and Bone metabolism : 2008;5(1): 49-56
31

3.Reverse phase:
The reverse cells whose role has not yet
been completely clarified performs this
phase. Indeed it is known that they are
macrophage like cells with a likely function
of removal of debris produced during matrix
degradation.

32

4.Formation phase:
Bone matrix resorption leads to the release of
several growth factors herein stored, including
bone morphogenetic proteins (BMPs),
fibroblast growth factors (FGFs) and
transforming growth factor β(TGF β), which are
likely responsible for the recruitment of the
osteoblasts in the reabsorbed area.

33

Once recruited, osteoblasts produce the new
bone matrix, initially not calcified (osteoid) and
then they promote its mineralization , thus
completing the bone remodeling process.
Unbalance between the resorption and
formation phases mirror an incorrect bone
remodeling , which in turn affects the bone
mass , eventually leading to a pathological
condition.

34

Bone remodelling process

Rucci, N.: Molecular biology of bone remodelling , Clinical cases
in Mineral and Bone metabolism : 2008;5(1): 49-56
35

Osteoblastogenesis process

36

Boskey, A.L., Coleman, R.: Aging and Bone. J Dental Res 2010 ; 89(12):
1333-1348
37

GROWTH FIELDS


Bone growth is controlled
by growth fields.



Distributed in a mosaic like
pattern across the surface
of a given bone.



They have pacemaking
function.



They are either resorptive
or depository activity.
38





About one half of the
bone is periosteal and
the other half
endosteal.
If endosteal surface is
resorptive then
periosteal surface
would be depository.

39

GROWTH SITES


Growth fields having
special role in the
growth of the particular
bone ( grows fast) are
called growth sites



e.g. mandibular condyle,
maxillary tuberosity,
synchondrosis of the
basicranium, sutures
and the alveolar
process.
41

GROWTH SITES


Baume proposed
the term growth site
for “regions of
periosteal or sutural
bone formation and
modeling resorption
adaptive to
environmental
influences.”

Koski, K. : Cranial growth centres: Facts or fallices?
, AJO-DO : Aug 1968: 566-583
42

GROWTH CENTERS


Special areas which
are believed to
control the overall
growth of the bone
e.g.mandibular
condyle.



Force, energy or
motor for a bone
resides primarily
within its growth
centre.

43

The term growth center is widely used in
connection with skeletal growth
phenomena.
Baume proposed that the term skeletal
growth center be used to describe “places
of endochondral ossification with tissue
separation forces.”

Koski, K. : Cranial growth centers: Facts or fallices? ,
AJO-DO : Aug 1968; 566-583
47

The definition proposed by Baume already
implies a spatial limitation that is a growth
centre includes only the territory where
endochondral ossification takes place .
The time element also appears important .

Koski, K. : Cranial growth centres: Facts or fallices? ,
AJO-DO :Aug 1968: 566-583,
45

Thus the growth centre should mean a place
where growth of the skeletal is occurring for a
sufficient length of time to make a real
contribution to the increase of the skeletal
mass beyond the size of the model tissue
existing at the onset of the growth centre
function.
AJO-DO : Aug 1968 : 566-583
46

A modified definition would be that a “
growth center is a site of endochondral
ossification with tissue separation forces ,
contributing to the increase of skeletal
mass.”

AJO-DO : Aug 1968: 566-583
47

PRINCIPLE OF ‘AREA RELOCATION’


Due to new bone
deposition on an
existing surface ,all
other parts of the
structure undergo
shifts in relative
position – a
movement
calledrelocation
48

As a result further adaptive bone
remodeling is necessary to adjust the
shape and size of the area to the new
relationship.

•Selective resorption and apposition
process functionally remodel the area to
conform to the new physiological loading.

49

ENLOW’S V PRINCIPLE


Most useful and basic
concept in facial growth
as many facial and
cranial bones have a Vshaped configuration.



Bone deposition(+)
occurs on the inner side
and resorption (-) occurs
on the outer surface.
50

EXAMPLE WITH V ORIENTED VERTICALLY


Bone deposition on
lingual side of
coronoid process ,

growth proceeds and
this part of the ramus
increases in vertical
dimension.
51

V ORIENTED HORIZONTALLY
 Same deposits of
bone also bring
about a posterior
direction of growth
movement.

 This produces a
backward movement
of coronoid processes
even though deposit is
on the lingual side
52



Same deposits carry base of bone in medial direction
.



So, the wider part undergoes relocation into a more
narrow part as the whole v moves towards the wide
part .

53

GROWTH MOVEMENTS


Two kinds of growth movements are seen
during the enlargement of craniofacial bases:
cortical drift & displacement.



CORTICAL DRIFT: All bones have one
common growth principle that is drift.



It was termed byEnlow(1963).



It is growth movement ( relocation or shifting)
of an enlarging portion of the bone by the
remodelling action of its osteogenic tissues.
54

DRIFT


It is remodeling
process and a
combination of
deposition and
resorption.



If an implant is placed
on depository side it
gets embedded.
Eventually marker
becomes translocated
from one side of
cortex to other.
55

The cortical plate can be relocated by
simultaneous apposition
&resorptionprocesess on the opposing
periosteal and endosteal surfaces.

The bony cortical plate drifts by depositing
and resorbing bone substances on the outer
& inner surfaces respectively in the direction
of growth.
56

If the resorption& deposition takes
place at the same times, the thickness
of the bone remains constant

Should more bone be deposited than
resorbed the thickness of the structure
increases

57

During the developmental period, deposition
takes place at a slightly faster rate than the
resorption , so that the individual bones slowly
enlarge.

The teeth follows the drift of the alveolae
while the jaw is growing & thus maintain their
position within the surrounding bony structure
despite the bone displacement.
58

DISPLACEMENT
It is the movement of the whole bone
as a unit.
It is a translatory movement of the
whole bone caused by surrounding
physical forces, and is the second
characteristics mechanism of skull
growth.
61

The entire bone is carried away from its
articular interfaces( sutures , synchondroses,
condyle) with adjacent bones.
Displacement is of two types namely:

Primary displacement- As a bone
enlarges , it is simultaneously carried away
from the other bones in direct contact with
it.This creates space within which bony
enlargement takes place.
62

It is the physical movement of the whole bone
,as the bone grows & remodels by resorption
and apposition.

63

Secondary displacement :It is the
movement of a whole bone caused by the
separate enlargement of other bones which
may be nearby or quite distant.

It is related to enlargement of other bone.
For example: growth in the middle cranial
fossa results in the movement of the
maxillary complex anteriorly& inferiorly .
64

TRAJECTORIES OF BONE
In 1867 an anatomist named Meyer, with
the help of the mathematician Culmann,
propounded the Trajectional theory of bone
formation.

He pointed out that the alignment of the
bony trabeculae in the spongiosa followed
definite engineering principles.
Graber T.M., Orthodontics-Principles and Practice. 3rd ed.
Philadelphia:Saunders;1992.p.133

66

If lines were drawn following discernible
columns of oriented bony elements, these
lines showed a remarkably similar structure
to the trajectories seen in a crane.
Many of these trajectories crossed at the
right angles – an excellent arrangement to
resist the manifold stresses on the condyle of
the femur.
67

In 1870’s Julius Wolff carried this theory one
step further. He claimed that the trabecular
alignment was due primarily to functional.
A change in the intensity and direction of
these forces would produce a demonstrable
change in the internal architecture and external
form or the bone.
This concept was referred to as “The law of
orthogonality”.

68

In essence , the law stated that the
stresses of tension or pressure on bone
stimulate bone formation.
Endochondral bone may respond
differently at its growth centre than
membranous bone.
69

It has been shown that both tension and
pressure can produce loss of bone tissue,
that the trabeculae do not form predominantly
straight lines .
Many of the so called trajectories are irregular
and wavy varying from bone to bone
depending on the stresses encountered .

70

Abnormal pressures on bone can cause
actual change , as seen on patients with
scoliosis who had been treated with
Milwaukee brace.
Benninghoff showed that the stress
trajectories obeyed no individual bone
limits , but rather the demand of the
functional forces
71

Changes in functional forces produces
measurable changes in bony architecture.
These changes are within the limit of
inherent morphogenetic pattern.
Lack of function leads to reduction of
density of bone tissue or osteoporosis.
Increased function produces a greater
density of bone in an area or osteosclerosis .
An example is kyphosis
72

TRAJECTORIES OF THE MAXILLA:

The presence of stress trajectories can
be demonstrated in the maxilla originating
from above the teeth and passing
superiorly to the zygomatic or jugal
buttress.
73

There are three main vertical trajectories,
all arising from the alveolar process and
ending in the base of the skull :
 The canine pillar .
 The zygomatic pillar .

 The pterygoid pillar

74

 Horizontal reinforcing members
include:

 Trajectories from:
 Hard palate, orbital walls ,
zygomatic arches , palatal bone &
lesser wing of sphenoid.


75

“Maxillary trajectories”

Horizontal
pillars

Vertical pillars

Canine
pillar

Malarzygo
matic pillar

Pterygoid
pillar

77

TRAJECTORIES OF THE MANDIBLE :

The mandible because it is a unit by itself
and a movable bone , has a different trabecular
alignment from that of the maxilla.

78

Trabecular columns radiate from the beneath
the teeth in the alveolar process & join together
in a common stress pillar or trajectory system,
that terminates in the mandibularcondyle .
The thick cortical layer of compact bone
along the lower border of the mandible
offers the greatest resistance to the
bending forces.
79

Other trajectory patterns are seen at the
symphysis , at the gonial angle & leading
downward from the coronoid process into
the ramus and body of the mandible.
These accessory stress trajectories
probably are due mainly to the direct
effect of the attachment of the muscles of
mastication.
80

Paradigm
It is a conceptual scheme that encompasses
individual theories and is accepted by a
scientific community as a model and
foundation for further research.

Moyers R.E.,Handbook of Orthodontics..4th ed. Year Book
Medical Publishers:1988.p.48-50
83

EVOLUTION OF PARADIGM‟S
Moyers R.E.,Handbook of Orthodontics..4thed.Year Book
84

Various paradigms
1920-1940
•Development of the Genomic Paradigm
• More emphasis on structure rather than function.
• Moss subdivided this period:
1. Preradiologic Phase-Emphasis placed
on craniometry
2. Radiological phase

Moyers R.E.,Handbook of Orthodontics..4thed.Year Book

85

Moss- “Classic Triad”
1. Sutures are primary growth sites
2. Growth of the cranial vault occurs
only by periosteal deposition and
endostealresorption.
3. All cephalic cartilages are primary
growth centers under direct genetic
control

86

1940-1960
•Craniofacial biology saw an increased emphasis
on experimental animal research in an effort to
account for the actual mechanism of facial growth.
•Studies were more methodological and
conceptual.
•Investigators began to recognize that there is
much more variation within the facial region and
that this variation could be the result of modifying
influences during Ontogeny
87

Technological developments:•Use of Radioopaque Implants.
• Vital Dyes.
• Autoradiography.
• In-vivo and In-vitro transplantations.
•By the end of 1950’s two similar approaches were
seen within the single Genomic Paradigm:
• Comprehensive Approach

•Structurofuntional Approach
88

Comprehensive Approach:
Continued with craniometrics but with
more sophisticated hardware including
radiographs,cephalostatsand software in the
form of statistical models.

Structurofunctional Approach:
Concentrated more on “cause and effect
relationships” within and among the biologic
systems of the Craniofacial complex.
89

By the end of 1950’s the genomic paradigm was put
into question
Periostealand Sutural bone growth were removed from
the genomic paradigm and given the status of
secondary, compensatory or adaptive phenomena
But due to lack of evidence the genomic paradigm
remained dominant and the alternative view that
“Function” plays a major role continued to gather
momentum.
90

MAINLY
DOMINATED
BY
GENOMIC
PARADIGM

91

1960-1980
Formulation of an Alternative paradigm.

--Termed as the “Functional Paradigm” stated that the
Craniofacial complex is highly adaptable to the
functional demands placed on it and its
developmental environment.
--Melvin Moss’s “Functional Matrix Hypothesis” is

believed by most craniofacial biologists to be the
alternative paradigm
92

DEVELOPMENT OF AN ALTERNATIVE PARADIGM
93

Moss 10 yrs later released a third paper on the same.
--From then on the “Functional” hypothesis became a
topic of theoretical debate involving people like:• Moorrees(1972)
• Johnston(1976)
• Koski(1977)
• Wayne Watson(1982)
Debate focused on:
• That cephalic cartilages have no intrinsic
growth properties.
• The mechanisms by which the capsular
matrices(oral,nasal,pharyngeal)assert
“morphogenic primacy”

94

--Alexander Petrovic and Associates(1975)
•Proposed the cybernetic models of
mandibular growth.

1980-2000
• This period saw a confluence of both the genomic
and the functional paradigms.
• A more focused view was developed and merits

and demerits of each theory were considered.
95

FUNCTIONAL
MATRIX
REVISITED

PRESENT

96

BONE REMODELLING THEORY
BY BRASH (1930)
This theory states that bone grows only by
interstitial growth.
The fundamental tenets of this theory are:
Bone grows only by apposition at the surface.
Growth of jaws takes place by deposition of bone at
the posterior surfaces of the maxilla and mandible.
This is described as Hunterian growth.
Carlson ,D.S.:Theories of craniofacial growrth in postgenomic era .
Seminorthod 2005;11:172-183

97

Calvarium grows through bone
deposition on the ectocranialsuface of the
cranial vault and resorption of bone on the
endocranial surface
Bone remodeling theory postulated that
the craniofacial skeletal growth takes place
by bone remodeling –selective deposition
and resorption of bone at its surfaces.

98

THE GENETIC THEORY( 1941)
Genetic theory was given by Brodie.

The genetic theory simply stated simply that
genes determine and control the whole
process of craniofacial growth.
But the mechanism of action by the genetic
unit and the mechanism by which the traits
are transmitted were not understood until
recently.
100

Genetic concept suggests that the genes
supply all the information in growth and
development.

 This originated with classical Mendelian
genetics.
Later with the blending of data from
vertebral paleontology created the neoDarwinian synthesis which is currently
accepted paradigm of phylogenetic
regulation.

101

Genetic concept stipulates that the
genotype supplies all the information
required for phenotypic expression.
Mossalso stated in his thesis that the
whole plan of growth, the various
operations carried out , the order and site
of growth and their co-ordination with
other systems are all embossed in the
nucleic acid message.
102

The field of genetics consists of two
principle areas :
“Transmission genetics” is characterized
by statistical approach and involved only in
explaining possible method of transmission.
It is based on Mendelian laws and did not
explain about genes or its characteristics.
103

THE SUTURAL HYPOTHESIS
Given by Sicher and Weinmann in 1947 .

According to this theory, sutures
,cartilages and periosteum are
responsible for facial growth and were
assumed to be under intrinsic genetic
control.
Sicher came to the conclusion that
sutures were causing most of the growth
based on the studies using vital dyes.
104

Essence of the Theory:
According to Sicher, the sutures are the
primary determinants of craniofacial growth.
The craniofacial skeleton enlarges due to
expansible forces exerted by the sutures as
they separate.

105

Theory:
He started that all bone forming elements like
sutures ,cartilages and periosteum are growth
centers like the epiphysis of the long bone.
Sicher called this theory as the sutural
dominance theory because he believed that the
primary event in sutural growth is proliferation of
the connective tissue between the two bones.
107

Proliferation of the sutural connective
tissue creates the space for appositional
bone growth between the borders of two
bones.

 Increase in the size of the cranial vault
takes place via primary growth of the bone at
the sutures, which forces the bones of the
vault away from each other.
108

Growth of the midface takes place via
intrinsically determined sutural expansion
of the circummaxillary suture system,
which forces the midface downward and
forward.
Mandibular growth takes place via
intrinsically determined growth of the
cartilage of the mandibularcondyle ,which
pushes the mandible downward and
forward.
109

There is considerable growth
occuring in suture and hence from this
point of view sutural growth attains
significance.

Sicher postulated that bone growth
within the various maxillary sutures
produces pushing of the bone which
results in forward and downward
movement of the maxilla.
110

It was believed that the stimulus for
bone growth is tension produced by
the displacement of the bones.

111

Koski (1968) stated there are two different
views regarding the structure of sutures.
Thefirst school or thought (Sicher and
Weinmann ) considers sutures as a
three layered structure.

Koski, K. : Cranial growth centres: Facts or fallices? , AJO-DO :
112
Aug 1968: 566-583

It stated that the connective tissue
between the two bones plays the same
role as the cartilage at the bases of the
skull and like epiphysis of the long bone
There is spreading of sutures due to
proliferation of middle layer of the sutural
tissue.
According to this concept tissue separating
force exists in the suture itself.
113

Thesecond school of thought (Pritchard
,Scott and Girgis,1956) says the suture as a
five layer structure .
 Each bone at the suture has its own two
layer of periosteum on both sides ant the
intervening fifth layer between these
periosteal layers.

114

This layer plays a role in adjustment
between the bones during the growth .
while the active proliferating role is
played by the cambial layers of the
periosteum of each bone.

115

It is very clear now from the histological
evidenced that the sutural structure is not
identical to that of the epiphyseal growth
plate.
Sicher also perceived the mandible as a
long bone and the mandibularcondylar
cartilage as comparable to epiphyseal plate
of the long bone.

116

EVIDENCES AGAINST SUTURAL
THEORY
 Trabecular pattern in the bones at the suture
change with age ,indicating the changes in the
direction of growth it cannot be accepted that
suture will have the necessary information for
altering growth.
Extirpation of facial sutures has no appreciation
effects on the dimensional growth of the skeleton
(Sarnat 1963)
118

Shape of sutures have been found to
depend on the functional stimulus.( Moss
&Salentejin, 1969)
Closure of sutures to be extrinsically
determined.( Moss ML, 1954)
Sutural growth can be halted by
mechanical forces like clips placed across
the sutures.
119

The parallelism of circummaxillary suture so as
to effect a forward and downward growth of maxilla
is only superficial .

Growth at zygomaticomaxillary suture occurs
predominantly in lateral direction .
The direction of growth of maxilla ranges from 0
to 82 degree in relation to SN plane .
It is practically impossible for the suture running
in same direction to push the maxilla parallel to the
reference plane. (Bjork 1966)
Bjork: Acta odont.scandinav.1966; 24:109-127

120

Conclusion:
Present evidences indicates suture as
adaptive growth sites.
Sutural tissues have no tissue separating
forces and they are not comparable to
growth centers.

121

NASAL SEPTUM
THEORY/CARTILAGENOUS
THEORY/NASOCAPSULAR THEORY
(1950)

James H Scott , an Irish anatomist in 1950
proposed the nasal septum theory as the
single and unified theory of craniofacial
growth.

122

Essence of theory:
According to this sutures play little role
or no direct role in the growth of the
craniofacial skeleton .
Sutures are considered as merely
passive secondary and compensatory
sites of bone formation and growth
123

After recognizing the importance of
cartilaginous parts of the head , nasal
capsule ,mandible and cranial base in
prenatal growth.

Scott felt that this cartilaginous
development was under genetic control
and was of the opinion that they continued
to dominate postnatal facial growth also.
124

Scott concluded that nasal septum is
mostly active and vital for craniofacial
growth both prenatally and postnatally.
The anterioinferior growth of the nasal
septal cartilage which is buttressed against
the cranial base “pushes” the midface
downward and forward.
The cranial base synchondroses causes
the growth of the cranial base and Scott
compared the condylar cartilage to the
cranial base cartilage

125

Discussion:
Numerous experimental studies were
conducted to address the validity of Scott’s
hypothesis .

This theory is based on the fact that
cartilage is a pressure adapted tissue and
expansion of cartilage provides the force to
displace downward and forwards.
126

According to Scott ,bone separation must
precede before the adaptive sutural bone
growth occurs .

The bone separation is because of growth
of organs like brain , eyeball or cartilage.

127

Scott is of the opinion that there are two suture
system:
 Posterior suture system lies behind the
maxilla and separates it from palatine ,lateral
mass of ethmoid , lacrimal , zygomatic and
vomer bones.

 Anterior suture system separates premaxilla
nasal and vomer bone.
128

 Scott said that the nasal cartilage is an
extension of the cranial base cartilage and
as it grows further, it separates the facial
bones from one another and also from the
cranial portion .
 Thus it allows bone growth to take place at
the sutures (frontomaxillary , frontonasal ,
frontozygomatic and
frontozygomaticomaxillary) by surface
deposition.
129

Evidences supporting the theory:
Experimental research on rats by Ohyama(1969) removal of septal cartilage produces deficient
growth of snout.

Also supported by research of Burdi , Petrovic ,
Baume,
Latham
respectively .

(1965,1967-1968,1968,1972)

130

EXPERIMENT BY BURDI , PETROVIC , BAUME,
LATHAM (1965,1967-1968,1968,1972)
RESPECTIVELY

131

 The importance of the septal growth
was also seen in impulse to maxillary
growth in cleft palate cases.
Failures of the underdeveloped
maxillary segment to unite with nasal
septum in complete unilateral clefts
deprives it of the growth impulse or
energy. The normal contra lateral side
on the other hand, attained normal
growth.
132

Sarnat in (1988)from experiments on rabbit
snout concluded that deformity of snout after
resection of nasal septum was the result of
lack of growth.
 Latham (1974) described the role of
septomaxillary ligament passing from
anterioinferior border of nasal septum to
anterior nasal spine and inter maxillary
suture in premaxillary region.

He stated that the traction through the
ligament will exert downward and forward
growth of maxilla.

133

Koski(1968) after histological study of nasal
septal cartilage found that there is
endochondral ossification taking place at
septoethmoidal junction.
Hunter and Enlow(1968) –in their growth
equivalent theory –emphasizes on relatively
lesser response of the endochondral cranial
base as opposed to immediate response of the
intramembranous cranial vault to external
influences
134

Evidence against the theory:
Moss and Bloonberg(1968), Brigit
Thilander(1970) found only slight deformity
after extirpation of septal cartilage
They concluded that septal cartilage
provides only mechanical support for the
nasal bones and is not a primary growth
center.
135

Two studies were carried out by Gilhus-Moe and
Lund in Scandinavia in 1960’s showed that
There are excellent chances that condylar
process would regenerate to approx. its
original size after trauma
In a few there was even a overgrowth of
condyle.
In a few children there is a reduction in growth
after injury maybe due to the trauma to the soft
tissues / scarring
Therefore Scott’s hypothesis does not hold true
completely.
136

CONCLUSION:
At present ,nasal septum theory is still
accepted as a reasonable explanation for
craniofacial growth.
 Nasal septum may be important
anterioposterior growth of face because of
endochondral growth process occurring at
its posterior border.

It is not considered to be an active
contributor for vertical development of face.
137

HUNTER &ENLOW’S GROWTH EQUIVALENT
The Hunter-Enlow growth equivalents
concepts is an important principle covering
the development of the facial skeleton.
As the individual components of the skull
develop in different directions ,they must
interact directly in order to compensate for
the carious growth activities,

This is achieved by growth equivalents
which act in opposing directions.
138

These growth equivalents coordinate the different
movements of the cranial base ,the
nasomaxillary complex and mandible , which are
due to development ,and thus determine the
adaptive changes in relation to individual parts of
the skull.

139

For example, elongation of the anterior cranial
base is related with enlargement of the
nasomaxillary complex.
Disturbances during realization of this growth
pattern cause craniofacial anomalies. The
disturbance can be related to disproportions of
the equivalents in the vertical or horizontal plane

140

THE FUNCTIONAL MATRIX THEORY
Introduction

Essence of theory
Explanation
Neurotrophism
Constraints of functional matrix
hypothesis

143

INTRODUCTION
The concept of this theory was
introduced first by Vander Klaww(194852).
Melvin L. Mossdeveloped the form and
function concept into the functional
matrix hypothesis.
Introduced in 1962.
144

ESSENCE OF THE THEORY

The functional matrix hypothesis claims that the origin
, form , position, growth and maintenance of all
skeletal tissues and organ are always secondary
,compensatory and necessary responses to
chronologically and morphologically prior events or
processes that occur in specifically related
nonskeletal tissues ,organs or functioning spaces
(functional matrices).

145

The hypothesis as shown that change
in size, shape, and location (growth) of
all craniofacial skeletal entities are
epigenetically( causally related series of
processes in external and internal
environment) regulated.

146

The epigenetic hypothesis suggests that the
post fertilization genome does not contain
sufficient information ,such as a blueprint, to
regulate all subsequent development.

As structural and functional complexity
increases new regulating information is
generated.

 The interaction of both genomic and
epigenetic factors is required to regulate or
cause development.

147

Proponents of the functional matrix states that the
expansion of the soft tissue matrix is primary and
the bone growth is purely secondary and
compensatory event.
Translation of the various bones of the face is due
to volumetric expansion of the encapsulated spaces
or tissues.

148

FUNCTIONAL CRANIAL COMPONENT

One function

Skeletal tissue

Neural tissue

Muscle tissue

Vascular tissue

Functional Cranial Component
151

Functional Cranial Component

Tissues and spaces that
completely perform a function

Functional matrix

A related skeletal unit that
acts biomechanically to
protect and/or support its
functional matrix

Skeletal cranial
component

1. Periosteal matrix
2. Capsular matrix
152

PERIOSTEAL MATRIX
Relates the matrix to those tissues that influence
the bone directly through the periosteum.
Examples of periosteal matrices includes:
Muscles.
Blood vessels and nerves lying in grooves or
entering or exiting through foramina.
Teeth.

153

Lack of contraction leads to atrophy of the bone.
All the periosteal matrices act homogeneously by
means of osseous deposition and resorption.
The muscles are attached either into the skeletal
tissue or indirectly by fusion with the outer fibrous
layer of periosteum.
Functioning muscles influence developmental
changes in the form of skeletal tissue to which they
are attached.

154

The periosteal matrices stimulation causes
growth of the micoskeletal units.

Affects a microskeletal unit, sphere of
influence is usually limited to a part of one bone
Temporalis – coronoid process.
Tooth

- alveolar bone.

They act to alter the size or shape or both
of the bones.
The growth process that occurs due to
periosteal matrix stimulation is called
Transformation.
155

CAPSULAR MATRIX
Included in this matrix are those masses
and spaces that are surrounded by
capsules.
Example:
Neural mass with scalp and dura.
Orbital mass with supporting tissues of
the eyes.

156

Capsules tend to influence macroskeletal
units which means portions of several bones
are simultaneously affected
Inner surface of calvarium.
This sharing of reaction by several
adjacent bones constitutes a
macroskeletal unit.

157

Each capsule is an envelope which
contains a series of functional cranial
components ,skeletal units and their
related functional matrices and is
sandwiched between two covering
layers.
Examples: neurocranial capsule
orofacial capsule

158

Neurocranial capsule:
In this cover consists of skin and
duramater ,the neurocapsular matrix
consists of the brain , leptomeninges
and CSF.

The expansion of the enclosed and
protected capsular matrix volume is
the primary event in the expansion of
the neurocranial capsule.
159

As the capsule enlarges ,the whole of the
included and enclosed functional
components, that is the periosteal
matrices and the microskeletal units are
carried outward in a totally passive
manner.
.

160

The calvarial functional cranial
components as a whole are passively
and secondarily translated in space.
In experimentally induced or
pathological states the periosteal
matrices are prevented from exerting
their morphogenetic activity.
161

The expansion of the neurocranial capsule
is proportional to the increase in neural
mass. This can be shown by considering
hydrocephaly as an example.
This suggests that the neural skull does not
grow first and thus provide space for the
expansion of the neural mass rather the
growth of neural mass is primary and
causes secondary compensatory growth of
the skull.
162

Thus the point is simple the neural skull does
not grow first and provide space for the
secondary expansion of the neural mass
rather the expansion of the neural mass is
primary event causing growth of the neural
skull.

163

Orofacial capsule:
All the functional cranial components of the
facial skull arise, grow and maintained
within the orofacial capsule.
This
surrounds
and
protects
the
orophoryngeal functioning spaces, and the
volumetric expansion of these spaces
serves as a primary morphogenetic extent
in facial skull growth.
Moss ML,SalentijinL.:The primary role of functional matrices in facial
growth: Am J Orthodjune 1969; 55;566-77
164

These spaces are left over as it were, when facial
bones, muscles blood vessels and nerves complete
their growth. The patency of these spaces are vital in
the metabolic demands of the body.

E.g. airway passage (accomplished by a dynamic
musculoskeletal postural balance the mechanism)
open masticatory cavity

165

SKELETAL UNITS
May be composed of bone, cartilage or
tendinous tissue. Each bone is
composed of several micro skeletal
units

The
possible
interaction
between
periosteal matrix and microskeletal units
includes
pterygoid
–
gonialangle,temporalis-coronoid
process, masseter
166

When the adjoining portions of a number of
neighboring bones are united to function as a
single cranial component it is termed as macroskeletal unit .

e.g. Endo cranial surface of the calvaria, maxilla,
mandible

The overall skeletal growth is a combination of
changes in microskeletal and macroskeletalunits
due to stimulation of periosteal and capsular
matrices respectively.
167

In the mandible we distinguish the following
micro skeletal units.


Coronoid micro skeletal unit –
functional demands of temporalis.



Angular micro skeletal unit – related to activity of
both masseter and medial pterygoid.



Alveolar unit – related to presence of teeth.



Basal micro skeletal unit – related to inferior
alveolar neurovascular bundle.

related

to

168

These micro skeletal units are relatively
independent of each other. The term functional
matrix is by no means implies only to soft
tissues
but
also
includes
muscles, glands, nerves, vessels fat, teeth etc.

Most of the orthodontic therapy is firmly based
on the fact that when this functional matrix
grows or is moved, the related skeletal unit
responds.
169

AGAINST
Spheno-occipital synchondrosis
Demonstrates autonomous growth

Nasal cartilage
Scott- midfacial growth not responsive to external
influence
Removal - deficient growth
Destruction of cell proliferation potential
without cicatrization – Deficient growth

Craniostenosis – premature stenosis of sutures
inhibits growth – sutures have some capacity to
regulate the activity of functional matrix
170

TRANSMISSION OF FUNCTIONAL STIMULUS TO THE
BONE-NEUROTROPHISM

Neurotrophism is a non impulsive
transmittiveneurofunction involving axoplasmic
transport providing for long term interaction
between neurons and innervated tissue , which
homeostatically regulate the morphological
compositional and functional integrity of those
tissues.

171

Types of neurotrophism:
1. Neuromuscular
2. Neuroepithelial
3. Neurovisceral
Neuromuscular trophism:
Neural innervations are established at
myoblast stage. The genetic control cannot
reside solely in the functional matrices alone
and there is neurotropically regulated
homeostatic control of genome and similar
neurotrophic mechanism exist for capsular
matrix which passively regulate the functional
cranial component.
172

Muscle denervation-reinnervation: muscle
denervation and reinnervation enable us
to diffrentiate effect on muscle tissue
associated with loss of impulse
conduction and contraction from those
due to loss of neurotrophic factors.
If motor neurons are sectioned and the
muscle subsequently becomes
reinnervated there is reformation of
neuronal conductive function, this
demonstrates neuromuscular trophism.
173

Neuroepithelialtrophism:
The neurological work of neurotrophism
first began in dermatology. The factors
which contribute to
neuroepithelialtrophism are:
1. local mechanism operating in areas of
high mitotic activity
2.Epithelial growth factors.

174

Neurotrophic control of genetic activity:
neurotrophic control of genetic activity
is demonstrated in many tissues under
experimental conditions:
Protein synthesis in oral epithelial cells
and specific enzymatic sysnthesis in
taste buds epithelium appear to be
neurotrophically regulated.

175

CURRENT CONCEPTS OF FMH:
THE MOLECULAR BASIS
The fmh failed to explain the sequences of
events through which the extrinsic stimuli
caused adaptive responses in the skeletal
structures i.e. the flow of the signals that
generated required response.
The new researches focused on intercellular
signaling, communication and signal
transduction from the molecular matrix to
micromolecular matrix.
176

CONCEPT OF MECHANOTRANSDUCTION
Mechanotransduction signifies cellular
signal transduction.
It is the process by which macromolecular
extrinsic stimuli are converted into cellular
signals, which can be internalized by a cell
and processed so that a suitable adaptive
response can be generated.
.
177

Altered external environment

Vital cells are pertrubed and leads to

Mechanoreceptors transmits an
extracellular physical stimulus into a
receptor cell

Mechantransduction –transduces or tarnsforms the
stimulus into an intracellular signal

Intracellular activation
179

OSSEOUS MECHANOTRANSDUCTION

It is a highly specialized and unique
mechanism by which bone cells
respond to extrinsic stimuli .It occurs in
single bone cells and bone cells are
computational elements that function
multicellularity as a connected cellular
network.

180

The unique nature is highlighted by the following
facts:
1. Unlike other mechanosensory cells ,bone cells
are not specialized for such stimuli
2. These cells shows aneural transmission of
signals
3. Bone cells show multiple adaptational
responses to a single force ,in contrast to
singular response by other tissue cells
4. The changes brought about by stimuli are
confined to a single bone to which the signal is
tarnsduced.
181

Osseous mechanotransduction translates the
periosteal functional stimulus into a skeletal unit
cell signal by two skeletal cellular
mechanotasductive process:
1. Ionic
2. Mechanical.
.

Ionic or electrical processes involves some form of
ionic transport through the bone cell plasma
membrane. The possible process includes stretch
activated ion channel ,electrokinetic and electric field
strengths .
182

The flow of these ions is thought to occur through the
voltage gated channels or gap junctions between the
adjacent osteocytes .The passage of K+ ,Ca+ ,Na+,
ions across the strained osteocytes have been
proved.

Electric field strength may also be a significant
parameter. Electrokinetic stimuli in the range of +2mv can initiate both osteogenesis and osteocytic
action potential

183

Mechanical process directly, without the
intracellular transductive process may itself be a
strong stimulus altering the cellular responses
through the the transmembrane molecule
integrin ,which may transduct the stimuli directly
into the nuclear membrane.
This cytoskeletal lever chain ,connecting to the
nuclear membrane may have the potential to
activate the osteocytic genome.

184

BONE AS AN OSSEOUS CONNECTED CELLULAR
NETWORK
•The term ccn implies a network exists between the
adjacent cells of a tissue through specialised
structures in the cell membranes.
•The specialized structures includes the tight
junction ,gap junctions in cell membrane. These
junctions spread stimuli very fast across the
connected cell.
•Extensive ccn exists in the bone and that the
principle component is the gap junction.
185

•Connexin 43 ,a cytoskeleton protein is the
major constituent this network.

•Gap juction not only connects the osteocytes to
the nighbouringosteocytes but the superficial
osteocytes to periosteal and
endostealosteoblasts too.

•Gap junction allows passage of ionic currents
molecules signals.
186

•All osteoblast are also interconnected
laterally.
•Vertically they connect
periostealosteoblast with
preosteoblastic cells and this in turn is
interconnected ,thus each ccn is like a
true syncytium and are electrically
active.
187

THE FMH AND EPIGENETICS
This concept of moss aims to find a middle path
to solve the controversy of genomic versus
epigenetic control of biologic processes.
Epigenetics is a term which includes : the sum
of all the biochemical, bioelectrical and
biophysical parameters-instantaneously present
intra ,inter and extracellularly- all of which are
produced by the functioning of the cell, tissue,
organ or organism itself.
188

It should be noted that these same
epigenetic factors serve as an internal
environment and must be considered
in addition to the classical external
environment of genetics.

Moss M.L.:The functional matrix hypothesis and
epigenetics:GraberT.M.:Physiologic principles of
functional appliances,STLouis;CV Mosby, 1985;3-4
189

It is postulated that epigenetic factors act
upon the products of the genome to
regulate all developmental processes
leading to the production ,increase and
maintenance of biological structural
complexity and provides feedback
regulation of genome itself.

190

•The fmh denies that the genome of
skeletogenic cells contain in and of itself
sufficient information to regulate the type,
site ,rate, direction and duration of
skeletal tissue growth.
•But to be sure the modern epigenticist
accepts both the data and fundamental
concepts of modern molecular biology.

191

In opposition epigenetics views the genome
as providing a set of formal prior intrinsic and
necessary causal factors which when
combined with efficient proximate extrinsic
and necessary epigenetic causal factors
together are sufficient to account the
regulation of development.

192

VAN LIMBORGH’S COMPROMISE
THEORY
Three major viewpoints considered:
Sicher’s
Scott’s
Moss’s

193

CONTROLLING FACTORS IN CRANIOFACIAL
GROWTH
INTRINSIC GENETIC
FACTOR

Genetic factors inherent to the
skull tissues

LOCAL EPIGENETIC
FACTORS

Genetically determined influence
originating from adjacent
structures and spaces ( brain,
eyes)

GENERAL
Genetically determined
EPIGENETIC FACTORS influences originating from
distant structures ( sex
hormones)
LOCAL
ENVIRONMENTAL
FACTORS

Local non genetic influences
originating from the external
environment( local external
pressure, muscle forces etc)

GENERAL
ENVIRONMENTAL
FACTORS

General non genetic influences
originating from external
environment ( food ,oxygen)

194

Sicher’s view
Cartilage
Sutures
Periosteum
Are all growth centers

195

Scott postulates
Intrinsic genetic factors affect:
Cartilage
Periosteum
while sutures are passiveandreactory.

197

Moss is felt to have erred
in denying any intrinsic genetic factors in the
control of chondrocranial growth and…
restricting the control of sutural growth to
local epigenetic and environmental factors.

199

VAN LIMBORG’S COMPROMISE
Chondrocranial growth is controlled by intrinsic
genetic factors
Desmocranial growth is controlled mainly by local
epigenetic factors
Desmocranial factors is also controlled by local
environmental factors
General epigenetic and general environmental
factors have very little role to play.
201

SERVO SYSTEM THEORY/CYBERNETICS
THEORY(1972)
 AlexandrePetrovic, explained that the growth of
various craniofacial regions is the result of
interaction of a series of causal changes and
feedback mechanisms.

 Based on a series of experiments , Petrovic
and coworkers have formulated a cybernetic
model for the control of mandibular growth.
203

Essence of the theory:
According to the theory ,control of primary
cartilages (mid face) takes a cybernetic form of
“command” whereas control of secondary
cartilages like condyle is comprised of both
direct effect of cell multiplication and also
indirect effects.

204

Simply stated, the servo system theory
is characterized by the following two
principal factors:
 (1) The horizontally regulated growth
of the midface and anterior cranial
base, which provide a constantly
changing reference input via the
occlusion

205

(2) the rate limiting effect of this midfacial
growth on the growth of the mandible.
While growth of the mandibularcondyle
and of the sutures may be affected directly
and indirectly by systemic hormones,
growth of these structures is clearly more
compensatory and adaptive to the action of
extrinsic factors, including local function as
well as the growth of other areas of the
craniofacial complex.
206

This theory starts with the explanation of
cybernetics.
 cybernetics is the science of control and
communication in the animal and
machine.

207

The theory postulates that every thing
affects everything and therefore
organized living systems never operate in
an open loop manner.
Open loop is a type of feedback
mechanism. The other type of feedback is
closed loop mechanism.

208

The feedback closes the regulation loop of
a given system in the following way..

209



According to cybernetics theory ,the
behaving organism is not seen as a
passive respondent called into action
by the changing environmental stimuli
but as a dynamic system which
continuously generates intrinsic activity
for organized interaction with the
environment.
210

Cybernetics in craniofacial growth:
cybernetics demonstrate the relationship
between observational and experimental
findings.

Black box: The physiologic system under
investigation is represented by the block
box .The contents of the black box is
usually not known.

211

Feedback signal:It is the function of
controlled variable that is compared to
the reference input
 It is negative in regulator and servo
system.


212







Closed loop system: If a physiologic
system is designed to maintain a specific
correspondence between inputs and
outputs, in spite of disturbance .
It is called as closed loop system .
It is characterized by the presence of a
feedback loop and comparator state.
213

Closed loop has two variations namely
regulator and servo system.
Open loop system has no feedback
loop or comparator.
The regulator: The main input is a
constant feature in this system .The
comparator detects disturbances and
their effects.

214

The servo system : It is also
called as follow up system .
 The main input is not a constant in
this system but varies across in
time.


215

Elements of the theory:
Command is a signal established
independently of the feedback system
under scrutiny.
It affects the behavior of the controlled
system without being affected by the
consequences of this behavior.

216

Examples :
 secretion rates of growth hormones ,
testosterone ,estrogen , stomatomedin.
They are not modulated by variations of
craniofacial growth.

217

o

References input elements : establish
the relationship between the command
and reference input. Includes septal
cartilage, septo-premaxillary
ligament, premaxillary and maxillary
bones.

o

Reference input is the signal established
as a standard of comparison ,eg. Sagittal
position of maxilla. Ideally it should be
independent of the feedback.
218

The controller is located between the
deviation signal and the actuating signal.
The confrontation between the position of
the upper and lower dental arch is the
comparator of the servosystem.

Activity of the retrodiscal pad and lateral
pterygod constitutes the actuating signals.
The elastic meniscotemporal and
meniscomandibularfrenum of the condylar
form the retrodiscal pad.
219

The controlled system is between the
actuator and controlled variable, i.e. growth
of the condylar cartilage through
retrodiscalpadstimulation.
Controlled variable is the output signal of
the servosystem . Best example is a
sagittal position of mandible.

220

The gain: the gain of a system is the
output divided by input . Gain value
greater than one it is called
amplification and if its less than one it is
called attenuation. The pterygocondylar
coupling is an example for gain

221

The disturbance: any input other than the
reference required is called a disturbance. It
results in deviation of the output signal .for
example: increase in hormone secretion
results in supplemental lengthening of
mandible.
The attractor: this is the final structurally
stable state in a dynamic system.
The repeller: this includes all unstable
equilibrium states like cusp to cusp occlusal
relationship.
222

Theory:

According to this the midface grows downward
and forward under the primary influence of the
cartilaginous cranial base and nasal septum ,
influenced principally by the intrinsic cell tissue
related properties common to all primary
cartilages and mediated by the endocrine system.
Carlson D.S.:Growthmodification:from molecules to mandible: reprinted from:
McNamara J.A.:Growthmodification:Whatworks,whatdosen,t and
why?,Craniofacial growth series 35,The University of Michigan,Ann Arbor,1999
223

The influence of somatotrophic hormones on
the growth of cartilages of nasal septum,
sphenooccipitalsynchondroses and other
follows that of a cybernetic form of
command pattern.

224

•Related to this event the maxillary dental arch
is carried into a slightly more anterior position.
this is the first and primary event.

•This causes a minute discrepancy between the
upper and lower arches ,which Petrovic referred
to as the comparator that is the constantly
changing reference point between the positions
of the dental arches.

225

Upper arch is the constantly changing
reference input.
Second propriorecptors within the
periodontal regions and TMJ perceive even
a very small occlusal discrepancy and
tonically activate the muscles responsible for
mandibular protrusion.

Petrovic says the functional appliances will
work in the same way when given to
stimulate mandibular growth in class 2
malocclusions.

226

Third activation of jaw protruding muscles
(retrodiscal pads and lateral pterygoid) acts
directly on the cartilage of the mandibularcondyle
and indirectly through the vascular supply to the
Tmj stimulating the condyle to grow.

The growth in secondary cartilage is like condyle
corresponds to local and environmental factors
(epigenetic control). Lower arches constitutes the
controlled variable

227

Finally the effect of the muscle function and
responsiveness of the condylar cartilage is influential
both directly and indirectly by the hormonal factors
acting principally on the condylar cartilage and on the
musculature.

228

This entire cycle is continuously activated as a
servomotor as long as the midface upper dental
arch continues to grow and mature and appropriate
extrinsic hormonal and functional factors remain
supportive .

This affects position of mandible .The
sagittalpostion of mandible depends on the
modification of condylar growth by the activity of
the retrodiscal pad and lateral pterygoid muscle
stimulation.

229

EVIDENCES AGAINST THE THEORY
•Goret-Nicaise, Awn (1983) found that the
resection of lateral pterygoid muscle fails to
diminish condylar growth.
•Das, Meyer, Sicher (1965) found that the
occlusion remained unaffected in
condylectomy studies.

230

CONCLUSION
Craniofacial growth and development are based to
large extent on evolving concepts .
At the start these concepts were based on naïve
assumptions about the perceived competing roles
of heredity and environment ,often framed within
the context of the age-old “nature nurture”
controversy.

231

The craniofacial biologist tend to believe that
there was a single ,overiding mechanism
governing the growth of the face and jaw tended
to focus on a search for what might be called the
HOLY GRAIL of CRANIOACIAL BIOLOGY, a
single theory that is both biologically accurate
and clinically effective.

232

REFERENCES
•Moyers R.E.,Handbook of Orthodontics..4thed.Year
Book Medical Publishers:1988.p.48-50
•Contemporary orthodontics-William.R.Proffit
,W.Fields,David.M.Sarver,5th edition
•Essential of faciial growth,3thed – H.Enlow, Hans

233

•Orthodontic diagnosis –Thomas Rakosi , I.Jonas ,
Thomas Graber ,1stediton

•Orthodontics diagnosis and management of
malocclusion and dentofacialdeformatiesO.P.Kharbanda 2nd edition

234

•Graber T.M., Orthodontics-Principles and Practice.
3rd ed. Philadelphia:Saunders;1992.p.133

•Moss ML.:Growth of the calvaria in the rats: The
determination of osseous morphology: Am J Anat
1954:94;333-62
•Sarnat BG:Postnatal growth of the upper
face:Some experimental considerations: The
Angle Orthodontist:1963 July:vol 33(3);139-61
235

•Das A, Meyer J, Sicher H: X-ray and alizarin
studies of the effect of bilateral condylectomy in
the rat : Angle Orthod: 1965;35;138-48

•Bjork, A: Acta odont.scandinav.1966; 24:109-127

•Koski, K. : Cranial growth centres: Facts or
fallices? , AJO-DO : Aug 1968: 566-583
236

•Sarnat BG:Postnatal growth of the nose and
face after resection of septal cartilage in the
rabbit.: Oral Surgery.,1968:26:712-727
•Ohyama K:Experimental study on growth and
development of dentofacial complex after resection
of cartilaginous nasal septum .Bull Tokyo
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237

•Goret-Nicaise,AwnM:Morphological effects on the rat
mandibularcondyle of section of the lateral
pterygoidmuscle:European J Orthod 1983;5;315-321

•Moss M.L:The functional matrix hypothesis and
epigenetics:GraberT..:Physiologic principles of
functional appliances,STLouis;CV Mosby, 1985;3-4

238

•Moss ML: The functional matrix hypothesis revisited
: part 2 the role of an osseous connected cellular
network.Am J OrthodDentofacialOrthop 1997;
112:221-6

•Moss ML:The functional matrix hypothesis
revisited: part 1.the role of
mechanotransduction.Am J
OrthodDntofacialOrthop 1997;112:8-11
•Carlson DS:Growthmodification:from molecules
to mandible: reprinted from: McNamara
J.A.:Growthmodification:Whatworks,whatdosen,t
and why?,Craniofacial growth series 35,The
University of Michigan,Ann Arbor,1999
239

•Carlson D.S:Theories of craniofacial growrth
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2005;11:172-183

•Rucci N: Molecular biology of bone remodelling
, Clinical cases in Mineral and Bone metabolism :
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•Boskey, A.L., Coleman, R: Aging and Bone. J
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240

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